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Differential release of mast cell interleukin-6 via c-kit
E Gagari, M Tsai, CS Lantz, LG Fox and SJ Galli
Department of Pathology, Beth Israel Deaconess Medical Center and Harvard
Medical School, Boston, MA 02215, USA.
Mast cells represent a potential source of interleukin-6 (IL-6) and other
cytokines that have been implicated in host defense, tissue
maintenance/remodeling, immunoregulation, and many other biologic
responses. In acquired immune responses to parasites or allergens, the
extensive IgE-dependent activation of mast cells via Fc epsilonRI can
result in the release of large quantities of biogenic amines that are
stored in the cells' cytoplasmic granules as well as the production of
lipid mediators and many cytokines; these products together can orchestrate
an intense inflammatory response. We now report that activation of mouse
mast cells via c-kit, the receptor for the pleiotropic survival/growth
factor, stem cell factor (SCF), can induce the release of IL-6. Upon
challenge with SCF, bone marrow-derived cultured mouse mast cells (BMCMCs)
released amounts of IL-6 that were greater than 100-fold more than those
produced by unstimulated cells, but that were substantially less than those
produced in response to IgE and specific antigen. Moreover, BMCMCs released
IL-6 upon challenge with concentrations of SCF that resulted in little or
no detectable release of tumor necrosis factor-alpha, leukotriene C4,
histamine, or serotonin. These findings indicate that SCF, a widely
expressed protein that is critical for mast cell development and survival,
can also regulate the differential release of mast cell mediators.
Volume 89,
Issue 8,
pp. 2654-2663,
04/15/1997
Copyright © 1997 by The American Society of Hematology
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